The objectives of this research are to identify etiological mechanisms which are operative in periodontal disease in vivo and to develop specific immunotherapeutic treatments for controlling periodontal disease. Gnotobiotic rats monoinfected with Actinomyces viscosus will be employed as a periodontal disease model. These animals will be immunized by various routes with individual Actinomyces viscosus antigens (1 antigen per rat) prior to monoinfection. Every major serologically delectable surface antigen produced by Actinomyces viscosus (a total of 12 antigens) will be used. The extent to which each rat develops humoral and cellular immune responses to individual antigens will be measured before monoinfection and at intervals after monoinfection as periodontal disease develops by determining serum and salivary immunoglobulin levels and by skin testing, respectively. By comparing immunized and unimmunized rats for their degree of periodontal disease and correlating disease severity with humoral and cellular immune responses to specific antigens, it will be possible to identify specific Actinomyces antigens and the immune responses they activate as either immunopathological (causing increased disease severity), or protective (causing decreased disease severity). These protective and destructive immune mechanisms will be fully characterized. All of the known Actinomyces serotypes will be screened by serological assays to determine which antigens are shared in common. Commonly shared antigens which activate protective immune responses will be used to develop a vaccine that will prevent the Actinomyces from causing periodontal disease. Alternatively it may be possible to treat periodontal disease by desensitizing the host to the harmful Actinomyces' antigens.